The Association of Blood Component Use Ratios With the Survival of Massively Transfused Trauma Patients With and Without Severe Brain Injury

Spinella, Philip C.; Wade, Charles E.; Blackbourne, Lorne H.; Borgman, Matthew A.; Zarzabal, Lee Ann; Du, Fei; Perkins, Jeremy G.; Maegele, Marc; Schreiber, Martin A.; Hess, John R.; Jastrow, Kenneth M.; Gonzalez, Ernest A.; Holcomb, John B.; Kozar, Rosemary A.

doi:10.1097/ta.0b013e318227ef2d

Cited by 49 publications

(34 citation statements)

References 14 publications

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“…However, the impact exerted by platelets on survival was not as strong as that of plasma transfusion [348,396], higher than the impact of plasma [355] or even absent, in contrast to the benefit of increased plasma:RBC ratios [401]. On the contrary, transfusion of a high platelet:RBC ratio and not a high plasma:RBC ratio was found to be associated with improved survival in patients with TBI [405]. …”

Section: Resultsmentioning

confidence: 99%

Management of bleeding and coagulopathy following major trauma: an updated European guideline

Bouillon²,

et al. 2013

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IntroductionEvidence-based recommendations are needed to guide the acute management of the bleeding trauma patient. When these recommendations are implemented patient outcomes may be improved.MethodsThe multidisciplinary Task Force for Advanced Bleeding Care in Trauma was formed in 2005 with the aim of developing a guideline for the management of bleeding following severe injury. This document represents an updated version of the guideline published by the group in 2007 and updated in 2010. Recommendations were formulated using a nominal group process, the Grading of Recommendations Assessment, Development and Evaluation (GRADE) hierarchy of evidence and based on a systematic review of published literature.ResultsKey changes encompassed in this version of the guideline include new recommendations on the appropriate use of vasopressors and inotropic agents, and reflect an awareness of the growing number of patients in the population at large treated with antiplatelet agents and/or oral anticoagulants. The current guideline also includes recommendations and a discussion of thromboprophylactic strategies for all patients following traumatic injury. The most significant addition is a new section that discusses the need for every institution to develop, implement and adhere to an evidence-based clinical protocol to manage traumatically injured patients. The remaining recommendations have been re-evaluated and graded based on literature published since the last edition of the guideline. Consideration was also given to changes in clinical practice that have taken place during this time period as a result of both new evidence and changes in the general availability of relevant agents and technologies.ConclusionsA comprehensive, multidisciplinary approach to trauma care and mechanisms with which to ensure that established protocols are consistently implemented will ensure a uniform and high standard of care across Europe and beyond.Please see related letter by Morel et alhttp://ccforum.com/content/17/4/442

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Section: Resultsmentioning

confidence: 99%

Management of bleeding and coagulopathy following major trauma: an updated European guideline

Bouillon²,

et al. 2013

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“…Previously, the effects of ARDS on clinical outcomes after TBI have been separately reported from studies of the association between transfusion of blood products and clinical outcomes after TBI(5, 6, 42–44). Interpreting our findings in the context of existing literature on TBI and transfusions is challenging because many of these studies either exclude isolated TBI or do not distinguish between TBI with and without polytrauma.…”

Section: Discussionmentioning

confidence: 99%

The acute respiratory distress syndrome following isolated severe traumatic brain injury

Hendrickson

Howard

Kornblith

et al. 2016

Journal of Trauma and Acute Care Surgery

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STRUCTURED ABSTRACT BACKGROUND Acute respiratory distress syndrome (ARDS) is common after Traumatic Brain Injury (TBI) and is associated with worse neurologic outcomes and longer hospitalization. However, the incidence and associated causes of ARDS in isolated TBI have not been well studied. METHODS We performed a subgroup analysis of 210 consecutive patients with isolated severe TBI enrolled in a prospective observational cohort at a Level 1 Trauma Center between 2005 and 2014. Subjects required endotracheal intubation and had isolated severe TBI defined by an Abbreviated Injury Score (AIS) Head ≥3 and AIS <3 in all other categories. ARDS within the first 8 days of admission was rigorously adjudicated using Berlin Criteria. Regression analyses were used to test the association between predictors of interest and ARDS. RESULTS The incidence of ARDS in the first eight days after severe isolated TBI was 30%. Patients who developed ARDS were administered more crystalloids (4.3 vs. 3.5 L, p= 0.005) and blood products in the first 12 hours of admission. Patients with ARDS had significantly worse clinical outcomes measured at 28 days, including longer median lengths of ICU and hospital stays (4 vs. 13 days, p<0.001, and 7.5 vs. 14.5 days, p<0.001, respectively). In unadjusted logistic regression analyses, the odds of developing ARDS were significantly associated with AIS Head score (OR 1.8, p=0.018), male sex (OR 2.9, p=0.012), and early transfusion of platelets 2.8 (p=0.003). These associations were similar in a multivariate logistic regression model. CONCLUSIONS In the era of balanced hemostatic resuscitation practices, severity of head injury, male sex, early crystalloids and early transfusion of platelets are associated with a higher risk of ARDS after severe isolated TBI. Early transfusion of platelets after severe TBI may be a modifiable risk factor for ARDS, and these findings invite further investigation into causal mechanisms driving this observed association. LEVEL OF EVIDENCE Level III; Epidemiologic

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“…Even if such tests are not readily available, our findings suggest maintaining a high index of suspicion for platelet dysfunction in isolated TBI patients and a low threshold for platelet transfusion if evidence of bleeding exists. 23-25,27 …”

Section: Discussionmentioning

confidence: 99%

Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats

Castellino

Chapman

Donahue

et al. 2014

Journal of Trauma and Acute Care Surgery

107

112

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BACKGROUND Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and depletion of coagulation factors. We hypothesized that the platelet dysfunction of CTBI is a distinct phenomenon from the coagulopathy following hemorrhagic shock. METHODS We used thrombelastography with platelet mapping as a measure of platelet function, assessing the degree of inhibition of the adenosine diphosphate (ADP) and arachidonic acid (AA) receptor pathways. First, we studied the early effect of TBI on platelet inhibition by performing thrombelastography with platelet mapping on rats. We then conducted an analysis of admission blood samples from trauma patients with isolated head injury (n = 70). Patients in shock or on clopidogrel or aspirin were excluded. RESULTS In rats, ADP receptor inhibition at 15 minutes after injury was 77.6% ± 6.7% versus 39.0% ± 5.3% for controls (p < 0.0001). Humans with severe TBI (Glasgow Coma Scale [GCS] score ≤ 8) showed an increase in ADP receptor inhibition at 93.1% (interquartile range [IQR], 44.8–98.3%; n = 29) compared with 56.5% (IQR, 35–79.1%; n = 41) in milder TBI and 15.5% (IQR, 13.2–29.1%) in controls (p = 0.0014 and p < 0.0001, respectively). No patient had significant hypotension or acidosis. Parallel trends were noted in AA receptor inhibition. CONCLUSION Platelet ADP and AA receptor inhibition is a prominent early feature of CTBI in humans and rats and is linked to the severity of brain injury in patients with isolated head trauma. This phenomenon is observed in the absence of hemorrhagic shock or multisystem injury. Thus, TBI alone is shown to be sufficient to induce a profound platelet dysfunction. (J Trauma Acute Care Surg. 2014;76: 1169–1176.

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The Association of Blood Component Use Ratios With the Survival of Massively Transfused Trauma Patients With and Without Severe Brain Injury

Cited by 49 publications

References 14 publications

Management of bleeding and coagulopathy following major trauma: an updated European guideline

Management of bleeding and coagulopathy following major trauma: an updated European guideline

The acute respiratory distress syndrome following isolated severe traumatic brain injury

Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats

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